Respiratory system mechanics in sedated, paralyzed, morbidly obese patients

Abstract

The effects of inspiratory flow and inflation volume on the mechanical properties of the respiratory system in eight sedated and paralyzed postoperative morbidly obese patients (aged 37.6 +/- 11.8 yr who had never smoked and had normal preoperative seated spirometry) were investigated by using the technique of rapid airway occlusion during constant-flow inflation. With the patients in the supine position, we measured the interrupter resistance (Rint,rs), which in humans probably reflects airway resistance, the "additional" resistance (delta Rrs) due to viscoelastic pressure dissipation and time-constant inequalities, and static respiratory elastance (Est,rs). Intra-abdominal pressure (IAP) was measured by using a bladder catheter, and functional residual capacity was measured by the heliumdilution technique. The results were compared with a previous study on 16 normal anesthetized paralyzed humans. Compared with normal persons, we found that in obese subjects: 1) functional residual capacity was markedly lower (0.645 +/- 0.208 liter) and IAP was higher (24 +/- 2.2 cmH2O); 2) alveolar-arterial oxygenation gradient was increased (178 +/- 59 mmHg); 3) the volume-pressure curve of the respiratory system was curvilinear with an "inflection" point; 4) Est,rs, Rint,rs, and delta Rrs were higher than normal (29.3 +/- 5.04 cmH2O/l, 5.9 +/- 2.4 cmH2O.l-1.s, and 6.4 +/- 1.6 cmH2O.l-1.s, respectively); 5) Rint,rs increased with increasing inspiratory flow, Est,rs did not change, and delta Rrs decreased progressively; and 6) with increasing inflation volume, Rint,rs and Est,rs decreased, whereas delta Rrs rose progressively. Overall, our data suggest that obese subjects during sedation and paralysis are characterized by hypoxemia and marked alterations of the mechanical properties of the respiratory system, largely explained by a reduction in lung volume due to the excessive unopposed IAP.

Physiologic correlates of dyspnea in patients with morbid obesity

“…These abnormalities are due to the effect of the abdominal content on diaphragm position. 8 A significant restriction was found in a minority of patients and was more frequent in patients with the highest BMI. However, the differences between the two groups did not reach statistical significance.…”

“…[4][5][6][7][8][9][10] The most frequent pulmonary function tests (PFTs) findings are reduced expiratory reserve volume (ERV), functional residual capacity (FRC) and total lung capacity (TLC), [4][5][6]9 which are generally related to alterations in chest wall mechanics induced by an increased abdominal load. 8 These alterations reduce total respiratory compliance. 7 The work of breathing is markedly increased in patients with severe obesity.…”

“…7 The work of breathing is markedly increased in patients with severe obesity. 11 Maximum voluntary ventilation as well as maximal inspiratory pressure (PImax) can also be low, [6][7][8][9][10] reflecting a decreased inspiratory muscle performance.…”

Problemas clínicos pré-anestésicos de pacientes morbidamente obesos submetidos a cirurgias bariátricas: comparação com pacientes não obesos

“…A presença de apnéia do sono agrava esta condição por causar redução da condutância respiratória nas vias aéreas superiores e inferiores, sobrecarregando os músculos da respiração 18 . Os anestésicos venosos e bloqueadores neuromusculares utilizados para a indução da anestesia provocam alterações na mecânica respiratória, principalmente aumento da resistência das vias aéreas, resultando em hipoxemia 19 . No paciente obeso, o aumento do volume de fechamento torna o tempo para a desnitrogenação alveolar mais longo e menor a tolerância à apnéia 20 .…”

Atelectasia pulmonar em cães durante anestesia geral

“…A CRF é menor em pacientes obesos, pois o gradiente de oxigenação alveolar-arterial (A-aDO 2 ) é maior, e a pressão intraabdominal é mais alta. Os diferentes mecanismos do sistema respiratório e a hipóxia encontrados nesses pacientes podem ser consequência da redução do volume pulmonar causada pela alta pressão intraabdominal (PELOSI et al, 1997). A formação de áreas de colapso alveolar pode ser encontrada em todas as idades (GUNNARSSON et al, 1991).…”